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  • Title: Shrinkage as a potential mechanism of recurrent clinical events in patients with a large vulnerable plaque.
    Author: Liu X, Sun C, Tian J, Liu X, Fang S, Xi X, Gu X, Sun Y, Tian J, Yu B.
    Journal: J Cardiovasc Med (Hagerstown); 2019 Aug; 20(8):518-524. PubMed ID: 30889077.
    Abstract:
    AIMS: This study aimed to investigate the progression and vascular shrinkage of vulnerable plaque lesions with a plaque burden at least 70% among patients with coronary artery disease by optical coherence tomography (OCT) and intravascular ultrasound (IVUS). METHODS: Fifty-six OCT-identified vulnerable plaques from 47 patients were included among coronary angiography-identified nonculprit/nontarget lesions. Serial IVUS images were used to assess plaque progression and vascular shrinkage. RESULTS: Thirty-five small vulnerable plaques (plaque burden <70%, group A) and 21 large vulnerable plaques (plaque burden ≥70%, group B) were identified. The IVUS results at baseline show that mean plaque areas (P < 0.001) and the percentage atheroma volume (PAV) (P < 0.0001) were greater and the minimal lumen area (P < 0.0001) was smaller in group B. The absolute and relative changes in the PAV and mean plaque area from baseline to follow-up were not significantly different. However, the lesions exhibited vessel shrinkage [the mean external elastic membrane (EEM) area (P = 0.02) and mean lumen area (P = 0.03) were significantly smaller in group B] from baseline to follow-up. Patients in group B also exhibited clinical events (recurrent angina symptoms) during the follow-up period. Positive correlations were found between changes in the mean plaque area and the mean EEM area in large vulnerable plaques (r = 0.61, P < 0.0001) and between changes in the mean EEM area and the mean lumen area in large vulnerable plaques (r = 0.61, P < 0.0001). CONCLUSION: Vulnerable plaque progression was not different between small and large vulnerable plaques. However, large vulnerable plaque lesions tended to exhibit vascular shrinkage, which is possible a cause of coronary artery lumen loss in patients with large vulnerable plaques.
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